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'''Foetal{{Short programming''' is a theorydescription|Theory that suggests thatenvironmental thefactors environmentduring of the foetus duringfetal development affects theiraffect disease risk later in life.risks}}
'''Fetal programming''', also known as '''prenatal programming''', is the theory that environmental cues experienced during fetal development play a seminal role in determining health trajectories across the lifespan.
The threeThree main routesforms of this programming arethat throughoccur due to changes in the maternal environment causingare:
* changesChanges in the development that leadslead to greater disease risk .;▼* geneticGenetic changes whichthat alter disease risk .;▼* [[Epigenetics| epigeneticEpigenetic]] changes which altersalter disease risk of not only theirthe child but theiralso children’sthat childrenof the next generation - i.e. , after a famine the, grandchildren of women who were pregnant during the famine, are born smaller than expectedthe evennormal withsize, thedespite returnnutritional ofdeficiencies normalhaving been nutritionfulfilled. ▼
These changes in the maternal environmental changes can be throughdue to nutritional changesalteration,<ref name = "Fleming_2012">{{cite journal | vauthors = Fleming TP, Velazquez MA, Eckert JJ, Lucas ES, Watkins AJ | title = Nutrition of females during the peri-conceptional period and effects on foetal programming and health of offspring | journal = Animal Reproduction Science | volume = 130 | issue = 3-43–4 | pages = 193–7 | date = February 2012 | pmid = 22341375 | doi = 10.1016/j.anireprosci.2012.01.015 }}</ref> hormonal changesfluctuations<ref>{{cite journal | vauthors = Talge NM, Neal C, Glover V | title = Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? | journal = Journal of Child Psychology and Psychiatry, and Allied Disciplines | volume = 48 | issue = 3-43–4 | pages = 245–61 | date = March 2007 | pmid = 17355398 | doi = 10.1111/j.1469-7610.2006.01714.x | pmc = 11016282 }}</ref> or exposure to toxins. ▼▲* changes in the development that leads to greater disease risk.
▲* genetic changes which alter disease risk.
▲* [[Epigenetics|epigenetic]] changes which alters disease risk of not only their child but their children’s children - i.e. after famine the grandchildren of women pregnant are born smaller than expected even with the return of normal nutrition.
▲These maternal environmental changes can be through nutritional changes,<ref>{{cite journal | vauthors = Fleming TP, Velazquez MA, Eckert JJ, Lucas ES, Watkins AJ | title = Nutrition of females during the peri-conceptional period and effects on foetal programming and health of offspring | journal = Animal Reproduction Science | volume = 130 | issue = 3-4 | pages = 193–7 | date = February 2012 | pmid = 22341375 | doi = 10.1016/j.anireprosci.2012.01.015 }}</ref> hormonal changes<ref>{{cite journal | vauthors = Talge NM, Neal C, Glover V | title = Antenatal maternal stress and long-term effects on child neurodevelopment: how and why? | journal = Journal of Child Psychology and Psychiatry, and Allied Disciplines | volume = 48 | issue = 3-4 | pages = 245–61 | date = March 2007 | pmid = 17355398 | doi = 10.1111/j.1469-7610.2006.01714.x }}</ref> or exposure to toxins.
== History ==
=== Dutch famine 1944–45 ===
In 1944–45, the German blockade of the Netherlands led to a lack of food supplies, causing the [[Dutch famine of 1944–45]]. The famine caused severe malnutrition among the population, including women in various stages of pregnancy. The Dutch Famine Birth Cohort Study examined the impact of lack of nutrition on children born during or after this famine. It showed that throughout their life, these children were at greater risk of [[Diabetes mellitus|diabetes]], [[cardiovascular disease]], [[obesity]], and other [[non-communicable disease]]s.{{citation needed|date=April 2023}}
=== DutchBarker famine 1944-45hypothesis ===
In the 1980’s1980s, [[David Barker (epidemiologist)|David Barker]] began a research study on this topic. The Barker Hypothesis, or [[Thrifty phenotype]], isforms the basis for much of the research conducted on foetalfetal programming. This hypothesis statedstates that if the foetusfetus is exposed to low nutrition , it will adapt to that environment. Nutrients are diverted totowards the developing heart, brain , and other essential fetal organs. The body also undergoes metabolic alterations that allow forensure survival withdespite low nutrition but may cause problems inwith normal or high nutrition.<ref>{{cite journal | vauthors = Remacle C, Bieswal F, Reusens B | title = Programming of obesity and cardiovascular disease | language = En | journal = International Journal of Obesity and Related Metabolic Disorders | volume = 28 Suppl 3 | issue = S3 | pages = S46-53 | date = November 2004 | pmid = 15543219 | doi = 10.1038/sj.ijo.0802800 | doi-access = free }}</ref> This leads to increased risk of developing [[metabolic syndrome]]. ▼In 1944-45 a German blockade led to a lack of food supplies in the Netherlands, which later became known as the [[Dutch famine of 1944–45|Dutch famine]]. This famine meant that the population became severely malnourished, including women in various stages of pregnancy.
== Nutritional status == ▼The Dutch Famine Birth Cohort Study looked at the effects of this lack of nutrition on the children born during or after this famine. Over the course of their lifetime it showed that they were at greater risk of diabetes, cardiovascular disease, obesity and other non-communicable diseases.
The developing foetusfetus gainsforms an impression of the world into which theyit will be born via its mother’smother's nutritional status ,. and itsIts development can beis thus modulated to provide it withcreate the best chance of survival. However, excessive or insufficient nutrition in the mother can provoke maladaptive developmental responses in the foetusfetus, which presentin asturn diseasesmanifest postnatally.in Itthe isform possibleof thatpost-natal diseases. This may hashave such a profound effect on the foetus’fetus’s adult life asthat toit can even outweigh lifestyle factors.<ref >{{cite journal | vauthorsname = Fleming"Fleming_2012" TP, Velazquez MA, Eckert JJ, Lucas ES, Watkins AJ | title = Nutrition of females during the peri-conceptional period and effects on foetal programming and health of offspring | journal = Animal Reproduction Science | volume = 130 | issue = 3-4 | pages = 193–7 | date = February 2012 | pmid = 22341375 | doi = 10.1016/ j.anireprosci.2012.01.015 }}</ref> ▼
=== Barker Hypothesis ===
▲In the 1980’s [[David Barker (epidemiologist)|David Barker]] began research on this topic. The Barker Hypothesis, or [[Thrifty phenotype]], is the basis for much of the research on foetal programming. This hypothesis stated that if the foetus is exposed to low nutrition it will adapt to that environment. Nutrients are diverted to the heart, brain and other essential organs. The body also undergoes metabolic alterations that allow for survival with low nutrition but cause problems in normal or high nutrition.<ref>{{cite journal | vauthors = Remacle C, Bieswal F, Reusens B | title = Programming of obesity and cardiovascular disease | language = En | journal = International Journal of Obesity and Related Metabolic Disorders | volume = 28 Suppl 3 | issue = S3 | pages = S46-53 | date = November 2004 | pmid = 15543219 | doi = 10.1038/sj.ijo.0802800 }}</ref> This leads to increased risk of developing [[metabolic syndrome]].
▲The developing foetus gains an impression of the world into which they will be born via its mother’s nutritional status, and its development can be thus modulated to provide it with the best chance of survival. However, excessive or insufficient nutrition in the mother can provoke maladaptive developmental responses in the foetus which present as diseases postnatally. It is possible that has such a profound effect on the foetus’ adult life as to even outweigh lifestyle factors.<ref>{{cite journal | vauthors = Fleming TP, Velazquez MA, Eckert JJ, Lucas ES, Watkins AJ | title = Nutrition of females during the peri-conceptional period and effects on foetal programming and health of offspring | journal = Animal Reproduction Science | volume = 130 | issue = 3-4 | pages = 193–7 | date = February 2012 | pmid = 22341375 | doi = 10.1016/j.anireprosci.2012.01.015 }}</ref>
=== Excessive nutrition ===
BMI[[Body priormass toindex]] before pregnancy, as well asand weight gain during pregnancy are both linked to high blood pressure in the offspring induring adulthood. Mouse models suggest that this is due to high foetal levels of the fetal hormone [[leptin]], which is prevalentpresent in the blood of individuals who are overweight or obese. ItThere is thoughta theory that this hormone hashurts a negative impact onthe regulatory systems inof the foetusfetus, suchand thatrenders it is impossible to maintain normal blood pressure within normal limitslevels. <ref>{{cite journal | vauthors = Taylor PD, Samuelsson AM, Poston L | title = Maternal obesity and the developmental programming of hypertension: a role for leptin | journal = Acta Physiologica | volume = 210 | issue = 3 | pages = 508–23 | date = March 2014 | pmid = 24433239 | doi = 10.1111/apha.12223 | s2cid = 22295003 | doi-access = free }}</ref>
=== Insufficient nutrition ===
[[Pre-eclampsia]], involving oxygen deprivation and death of the [[Trophoblast|trophoblastic cells]] makingthat make up most of the placenta, is a disease which is often associated with the maladaptive long-term consequences of inappropriate foetalfetal programming. Here, aan poorlyinadequately developed and poorly functioning placenta fails to meet the foetus’fetus’s nutritional needs during gestation, either by altering its selectivityselection for nutrients whichthat can cross into foetalfetal blood or restricting total volume thereof. The consequencesConsequences of this for the foetusfetus in adult life include cardiovascular and metabolic conditions. <ref>{{cite journal | vauthors = Myatt L | title = Placental adaptive responses and fetal programming | journal = The Journal of Physiology | volume = 572 | issue = Pt 1 | pages = 25–30 | date = April 2006 | pmid = 16469781 | pmc = 1779654 | doi = 10.1113/jphysiol.2006.104968 }}</ref>
== Hormonal influence ==
A delicate balance of hormones during pregnancy is thoughtregarded as highly relevant to foetalfetal programming and may significantly influence offspringthe outcomesoutcome of the offspring.<ref name=":0Hoffman_2016">{{cite journal | vauthors = Hoffman MC | title = Stress, the Placenta, and Fetal Programming of Behavior: Genes' First Encounter With the Environment | journal = The American Journal of Psychiatry | volume = 173 | issue = 7 | pages = 655–7 | date = July 2016 | pmid = 27363547 | doi = 10.1176/appi.ajp.2016.16050502 | doi-access = free }}</ref> Placental endocrine transfer from the mother to the developing foetusfetus could be altered by the mental state of the mother, due to affected [[glucocorticoid]] transfer that takes place across the placenta.<ref name=":0Hoffman_2016" />
=== Thyroid ===
Thyroid hormones haveplay an essentialinstrumental role during the early development of the foetusfetus's brain;. thereforeTherefore, mothers suffering from thyroid-related diseaseissues and the consequent altered thyroid hormone levels, may encourageinadvertently trigger structural/ and functional changes toin the foetalfetal brain. theThe foetusfetus is able tocan produce its own thyroid hormones from the beginningonset of the second trimester,; however, maternal thyroid hormones are important for brain development before and after the baby iscan able to synthesisesynthesize the hormones while still in uterothe uterus.<ref name=":1Andersen_2016">{{cite journal | vauthors = Andersen SL, Olsen J, Laurberg P | title = Foetal programming by maternal thyroid disease | journal = Clinical Endocrinology | volume = 83 | issue = 6 | pages = 751–8 | date = December 2015 | pmid = 25682985 | doi = 10.1111/cen.12744 | s2cid = 32873121 | doi-access = free }}</ref> TheDue to this, the baby may experience an increased risk of neurological or psychiatric diseasediseases later in their life.<ref name=":1Andersen_2016" />
=== Mental stateCortisol ===
Cortisol (and glucocorticoids more generally) is the most well-studied hormonal mechanism that may have prenatal programming effects.<ref>{{cite journal | vauthors = Moisiadis VG, Matthews SG | title = Glucocorticoids and fetal programming part 2: Mechanisms | journal = Nature Reviews. Endocrinology | volume = 10 | issue = 7 | pages = 403–11 | date = July 2014 | pmid = 24863383 | doi = 10.1038/nrendo.2014.74 | s2cid = 11475810 }}</ref> Although cortisol has normative developmental effects during prenatal development, excess cortisol exposure has deleterious effects on fetal growth,<ref>{{cite journal | vauthors = O'Donnell KJ, Meaney MJ | title = Fetal Origins of Mental Health: The Developmental Origins of Health and Disease Hypothesis | journal = The American Journal of Psychiatry | volume = 174 | issue = 4 | pages = 319–328 | date = April 2017 | pmid = 27838934 | doi = 10.1176/appi.ajp.2016.16020138 | doi-access = free }}</ref> the postnatal function of physiological systems such as the hypothalamic-pituitary-adrenal axis <ref>{{cite journal | vauthors = Kapoor A, Petropoulos S, Matthews SG | title = Fetal programming of hypothalamic-pituitary-adrenal (HPA) axis function and behavior by synthetic glucocorticoids | journal = Brain Research Reviews | volume = 57 | issue = 2 | pages = 586–95 | date = March 2008 | pmid = 17716742 | doi = 10.1016/j.brainresrev.2007.06.013 | s2cid = 30865698 }}</ref> and brain structure or connectivity (e.g., amygdala).<ref>{{cite journal | vauthors = Buss C, Davis EP, Shahbaba B, Pruessner JC, Head K, Sandman CA | title = Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 20 | pages = E1312-9 | date = May 2012 | pmid = 22529357 | pmc = 3356611 | doi = 10.1073/pnas.1201295109 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Graham AM, Rasmussen JM, Entringer S, Ben Ward E, Rudolph MD, Gilmore JH, Styner M, Wadhwa PD, Fair DA, Buss C | display-authors = 6 | title = Maternal Cortisol Concentrations During Pregnancy and Sex-Specific Associations With Neonatal Amygdala Connectivity and Emerging Internalizing Behaviors | journal = Biological Psychiatry | volume = 85 | issue = 2 | pages = 172–181 | date = January 2019 | pmid = 30122286 | pmc = 6632079 | doi = 10.1016/j.biopsych.2018.06.023 }}</ref>
The mental state of the mother during pregnancy is able to affect the foetus in utero, predominantly via hormones and genetics.<ref name=":2">{{Cite web|url=https://academic-oup-com.ezproxy.is.ed.ac.uk/molehr/article/19/1/1/1034162|title=EASE|website=academic-oup-com.ezproxy.is.ed.ac.uk|language=en|access-date=2018-09-26}}</ref> The mother's mood including maternal prenatal anxiety, depression and stress during pregnancy correlates with altered outcomes for the child.<ref name=":2" /> Although, not every foetus exposed to these factors is affected in the same way to the same degree, therefore genetic and environmental factors are suspected to significantly influence.<ref name=":2" /> ▼
During gestation, cortisol concentrations in maternal circulation are up to ten times higher than cortisol concentrations in fetal circulation.<ref>{{cite journal | vauthors = Travers S, Martinerie L, Boileau P, Xue QY, Lombès M, Pussard E | title = Comparative profiling of adrenal steroids in maternal and umbilical cord blood | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 178 | pages = 127–134 | date = April 2018 | pmid = 29191401 | doi = 10.1016/j.jsbmb.2017.11.012 | s2cid = 3705475 }}</ref> The maternal-to-fetal cortisol gradient is maintained by the placenta, which forms a structural and enzymatic barrier to cortisol.<ref>{{cite journal | vauthors = Chapman K, Holmes M, Seckl J | title = 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action | journal = Physiological Reviews | volume = 93 | issue = 3 | pages = 1139–206 | date = July 2013 | pmid = 23899562 | pmc = 3962546 | doi = 10.1152/physrev.00020.2012 }}</ref><ref>{{cite journal | vauthors = Stirrat LI, Sengers BG, Norman JE, Homer NZ, Andrew R, Lewis RM, Reynolds RM | title = Transfer and Metabolism of Cortisol by the Isolated Perfused Human Placenta | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 103 | issue = 2 | pages = 640–648 | date = February 2018 | pmid = 29161409 | pmc = 5800837 | doi = 10.1210/jc.2017-02140 }}</ref> During the first two trimesters of gestation intrauterine cortisol is primarily produced by the maternal adrenal glands.<ref name="Development and function of the hum">{{cite journal | vauthors = Ishimoto H, Jaffe RB | title = Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit | journal = Endocrine Reviews | volume = 32 | issue = 3 | pages = 317–55 | date = June 2011 | pmid = 21051591 | pmc = 3365797 | doi = 10.1210/er.2010-0001 }}</ref> However, during the third trimester the fetal adrenal glands begin to endogenously produce cortisol and become responsible for most intrauterine cortisol by the time the fetus reaches term.<ref name="Development and function of the hum"/>
Maternal depression is one of the greatest risks for increased vulnerability to adverse outcomes for a developing baby in the uterus, in particular susceptibility to a variety of psychological conditions.<ref name=":3">{{cite journal | vauthors = Davis EP, Hankin BL, Swales DA, Hoffman MC | title = An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? | journal = Development and Psychopathology | volume = 30 | issue = 3 | pages = 787–806 | date = August 2018 | pmid = 30068416 | doi = 10.1017/S0954579418000470 }}</ref> The mechanisms able to explain the connection between maternal depression and the offspring's future health are mostly unclear and a current area of active research.<ref name=":3" /> Genetic inheritance making the child more susceptible may play a role, including the effect on the intrauterine environment for the baby whilst the mother suffers from depression.<ref name=":3" /> ▼
== Psychological stress and psychopathology ==
==== Stress ====
▲The mentalMental state of the mother during pregnancy is able to affectaffects the foetusfetus in uterothe uterus, predominantly via hormones and genetics.<ref name=" :2Suter_2013">{{ Citecite journal web| url vauthors = https://academic-oup-com.ezproxy.is.ed.ac.uk/molehr/article/19/1/1/1034162 Suter MA, Anders AM, Aagaard KM | title = EASE Maternal smoking as a model for environmental epigenetic changes affecting birthweight and fetal programming | website journal = academic-oup-com.ezproxy.is.ed.ac.uk Molecular Human Reproduction | language volume = en 19 | access- issue = 1 | pages = 1–6 | date = 2018-09-26 January 2013 | pmid = 23139402 | pmc = 3521486 | doi = 10.1093/molehr/gas050 }}</ref> The mother's mood , including maternal prenatal anxiety, depression and stress during pregnancy correlates with altered outcomes for the child.<ref name=" :2Suter_2013" /> AlthoughThat being said, not every foetusfetus exposed to these factors is affected in the same way and to the same degree, thereforeand genetic and environmental factors are suspectedbelieved to significantlyhave a significant degree of influence.<ref name=" :2Suter_2013" />
Stress suffered by the mother during pregnancy can have effects to the developing baby including early labour, low birth weight and induce a risk for later psychiatric complications later in life.<ref name=":0" /> There are also effects to the mother, such as postpartum depression and consequently, finding new parenting more difficult compared to those who did not experience so much stress during their pregnancy.<ref name=":0" />
▲Maternal depression isposes one of the greatest risks for increased vulnerability to adverse outcomes for a developing baby that is developing in the uterus, especially in particularterms of susceptibility to a variety of psychological conditions.<ref name=" :3Davis_2018">{{cite journal | vauthors = Davis EP, Hankin BL, Swales DA, Hoffman MC | title = An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression? | journal = Development and Psychopathology | volume = 30 | issue = 3 | pages = 787–806 | date = August 2018 | pmid = 30068416 | pmc = 7040571 | doi = 10.1017/S0954579418000470 }}</ref> TheMechanisms mechanismsthat able tomay explain the connection between maternal depression and the offspring's future health are mostly unclear and form a current area of active research.<ref name=" :3Davis_2018" /> Genetic inheritance makingthat may be rendering the child more susceptible may play a role, including the effect on the intrauterine environment for the baby whilst the mother suffers from depression.<ref name=" :3Davis_2018" />
=== Psychological stress ===
Maternally experienced psychological stress that occurs either before or during gestation can have intergenerational effects on offspring. Stress experienced during gestation has been linked with preterm delivery, low birth weight, and increased risk of psychopathology.<ref name="Hoffman_2016" /> The new mother may suffer from after-effects too, such as postpartum depression, and subsequently may find parenting more difficult as compared to those who did not experience as much stress during their pregnancies.<ref name="Hoffman_2016" />
== Toxins ==
Toxins such as alcohol, tobacco, and certain drugs exposed to which the baby is exposed during theirits development are thought to contribute to foetalfetal programming, especially via alterations to the HPA axis.<ref name=":4Bekdash_2014">{{cite journal | vauthors = Bekdash R, Zhang C, Sarkar D | title = Fetal alcohol programming of hypothalamic proopiomelanocortin system by epigenetic mechanisms and later life vulnerability to stress | journal = Alcoholism,: Clinical and Experimental Research | volume = 38 | issue = 9 | pages = 2323–30 | date = September 2014 | pmid = 25069392 | pmc = 4177357 | doi = 10.1111/acer.12497 }}</ref> EspeciallyIf ifthe exposedexposure tooccurs during a critical windowphase of foetalfetal development, thisit iscould thoughthave todrastic exertand mostdire consequenceconsequences for the foetusfetus.<ref name=":4Bekdash_2014" />
=== Alcohol ===
Prenatal and/or early postnatal exposure to alcohol (ethanol) has been found to exerthurt negative effects ona child's neuroendocrine and behaviouralbehavioral factors.<ref name=":5Weinberg_2008">{{cite journal | vauthors = Weinberg J, Sliwowska JH, Lan N, Hellemans KG | title = Prenatal alcohol exposure: foetal programming, the hypothalamic-pituitary-adrenal axis and sex differences in outcome | journal = Journal of Neuroendocrinology | volume = 20 | issue = 4 | pages = 470–88 | date = April 2008 | pmid = 18266938 | doi = 10.1111/j.1365-2826.2008.01669.x | pmc = 8942074 | s2cid = 4574957 }}</ref> Alcohol passes through the placenta, throughon being ingestioningested by the mother during her pregnancy, and ismakes accessedits byway to the baby ''in utero''.<ref name=":5Weinberg_2008" /> the changesChanges posed to the foetusfetus bythrough ethanol exposure may significantly effect growth and development; these disordersare constitutecollectively foetalknown as fetal alcohol spectrum disorders (FASD).<ref name=":5Weinberg_2008" /> The exact interactionsinteraction between ethanol and the developing foetusfetus areis complex and largely uncertain, however, there are thought to be bothseveral direct and indirect effects onhave abeen developing babyobserved as itthe fetus developsmatures.<ref name=":5Weinberg_2008" /> Predominant effectsamong these are thoughtirregularities to bein the foetusfetus's endocrine, metabolic, and physiological functions.<ref name=":5Weinberg_2008" />
=== Smoking ===
The negative consequences of [[smoking]] are well-known, although theand consequencesthese may be even more apparent during pregnancy.<ref name=":6Suter_2013">{{Cite web|url=https://academic-oup-com.ezproxy.is.ed.ac.uk/molehr/article/19/1/1/1034162|title=EASE|website=academic-oup-com.ezproxy.is.ed.ac.uk|language=en|access-date=2018-09-26}}</ref> Exposure to tobacco smoke during pregnancy, commonly known as ''in utero'' maternal tobacco smoke exposure (MTSE), can contribute totowards thevarious differentproblems response ofin babies of smoking mothers.<ref name=":6Suter_2013" /> About 20% of mothers smoke whilst pregnant and this is associated with increased risk of complications, forsuch exampleas preterm birth, decreased foetalfetal growth leading to decreasedlower birth weight, and impaired fetal lung development of the baby whilst they develop in the womb.<ref name=":6Suter_2013" />
=== Drugs ===
There is evidence forpointing towards pharmacological programming of the fetus during the first trimester: foetal programming.<ref name=":7Bayliss_2002">{{cite journal | vauthors = Bayliss H, Churchill D, Beevers M, Beevers DG | title = Anti-hypertensive drugs in pregnancy and fetal growth: evidence for "pharmacological programming" in the first trimester? | journal = Hypertension in Pregnancy | volume = 21 | issue = 2 | pages = 161–74 | date = January 2002 | pmid = 12175444 | doi = 10.1081/prg-120013785 | s2cid = 30016072 }}</ref> One suchtype drugof typedrugs which is suspected toof influenceinfluencing the developing baby are anti-hypertensive drugswhen used during pregnancy is anti-hypertensive drugs.<ref name=":7Bayliss_2002" /> Pre-eclampsia (a conditionalcondition of hypertension during pregnancy), is a serious problemsproblem for the proportionmajority of pregnant mothers and can predispose the mother to a variety youof complications, including increased risk of mortality and problems during parturition.<ref name=":7Bayliss_2002" />
== References ==
{{Reflist}}
<references />
▲== External Linkslinks ==
* [https://www.southampton.ac.uk/populationhealth/research/mrc_lifecourse_epidemiology.page MRC Lifecourse Epidemiology Unit page at the University of Southampton]
* [https://www.cfp-research.com/About%20CFP/About%20fetal%20programming.aspx Fetal Programming page on the Centre for Fetal Programming's website.]
[[Category:Women's health]]
[[Category:Human pregnancy]]
[[Category:Epigenetics]]
▲[[Category: MedicineEmbryology]]
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